000) with progression from mild to severe dysplasia. The prevalence of cyclin D1 over expression varied from weak in low-grade lesions to intense staining in higher grades of epithelial selleck Erlotinib dysplasia. The cyclin D1 staining in the precursor lesions was mostly seen in suprabasal cell layers[52] and also an increased expression is observed in the parabasal and superficial layers of oral leukoplakias. Hence, this marker is considered useful and sensitive, and it is able to differentiate both normal epithelium from low grade dysplasia and low grade dysplasia from high grade dysplasia. The first study to demonstrate the association between the cyclin D1 expression and the risk of premalignant lesions was performed by Huang et al.
in 2006 and they found a significant increase in the expression of cyclin D1 with progression of the potentially malignant lesions towards malignancy, which is similar to the results of our study.[53] Furthermore, because of the higher number of cells and the relatively high proliferative activity in dysplastic leukoplakias, the superficial layer and the basal layer seem to be the most adequate tissue components in which to investigate the possible modulation of cell proliferation in precursor lesions treated with chemopreventive agents.[44] It has been substantiated that the overexpression of cyclin D1 leads to shortened duration of the G1 phase and reduced growth factor dependency. Therefore, deregulated expression of the cyclin D1 can cause disturbances in cell cycle control and normal mitogenicsignaling pathways, which contribute to cell transformation and tumorigenesis.
[54,55] p27 which was first identified as a cyclin dependant kinase inhibitor due to its ability to block the activity of cyclin E/cdk2 and cyclin A/cdk2 in cells arrested in G1 phase, was the other marker used in our study. A large number of studies have examined the diagnostic and prognostic significance of p27 expression in various tumors. Low p27 expression was also associated with increasing lymph node metastasis and stage of tumor and resulted in a poor prognosis for patients with oral tongue squamous cell carcinoma. p27 is apparently a significant predictor of survival.[56] Many studies have demonstrated a decrease in the expression of p27 protein in dysplasias compared with the non-dysplastic epithelium along with a trend of decreasing p27 levels with increasing grades of dysplasia.
[57] Whether the changes in p27 protein seen in epithelial dysplasias and carcinomas are a primary event or are simply a consequence of increased cell proliferation has yet to be determined.[58,59] A significant decrease in expression of p27 (P < 0.012) Drug_discovery with the progressive grades of dysplasia was observed in our study, which suggests that reductions in p27 protein may contribute to, or reflect, the increased cell proliferation seen in any progression towards oral carcinoma and early carcinogenesis.
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